Prevalence and Clinical Correlates of Thirdhand Smoke Exposure in a Pediatric Patient Population

项目摘要 三手烟是烟草烟雾污染物的持久性有毒残留物， 表面，留在灰尘中，并成为嵌入环境中，二手烟（SHS） 被释放到空气中。即使当父母努力保护他们的孩子远离烟草时， 吸烟、暴露于SHS（SHSe）和THS（THSe）仍然发生。以前吸烟的烟草残留物， 在家中或汽车中产生了一个无处不在的烟草烟雾污染物储存库， 手，如地毯，家具，衣服和玩具，并吸入灰尘。吸烟者的家庭成为 这些污染物的水库，持续多年，变得更加有毒，随着年龄的增长，后来重新排放到 气相中，或与常见的环境氧化剂和其他环境化合物反应，以产生二次 致癌的烟草特有的亚硝胺等污染物。THSe的临床效果尚不清楚 因为之前的研究已经调查了暴露于SHS和THS的儿童。专门研究 这些都是需要的。因此，我们进行了体外、动物和试点儿科研究，证明 THSe与高水平的炎性细胞因子、呼吸系统疾病和氧化应激有关 包括DNA损伤。我们发现，即使在禁烟令的存在下， 他们手上的THS污染水平很高，而不吸烟者的家中有很高的THS污染水平。然而，在这方面， 在缺乏大规模、严格的人体研究的情况下，无法得出有关THSe临床效果的结论 进行了因此，我们提出了一个创新的前瞻性纵向队列研究，将推动该领域的发展 从实验室到儿科临床环境，这是第一个使用生物化学的儿科研究， 验证，以确定儿童暴露于THS-只随着时间的推移。我们将筛选1000名儿童， 急诊科，一个照顾不同烟草烟雾暴露（TSE）水平的儿童的环境 和疾病。使用严格的筛选和化学分析技术，我们将识别和比较儿童 包括三个不同TSE组：1）仅TSE组：与非吸烟者一起生活，未报告SHSe， 证实SHSe阴性/低水平，THSe水平升高; 2）混合SHSe+THSe组： 吸烟者、报告的SHSe、证实的中/高水平的SHSe、高水平的THSe;以及3）无TSE组： 与不吸烟者一起生活，没有报告SHSe，证实SHSe和THSe水平为阴性。患病率和 这些群体的THSe水平、人口统计学、暴露和疾病模式将随着时间的推移进行比较。 接下来，我们将解开哪些环境源有助于THSe水平以及与THSe水平之间的关联。 THSe和炎症（即，细胞因子）和氧化（即，DNA、脂质、蛋白质氧化）生物标志物和TSE- 相关临床疾病。结果将提供独特的见解如何THSe和来源的烟草烟雾 污染影响儿童的炎症、氧化和临床反应。这些潜在影响 研究结果是实质性的，因为目前，THSe的临床风险水平尚不清楚。

PROJECT SUMMARY Thirdhand smoke (THS) is the persistent toxic residue of tobacco smoke pollutants that attaches to surfaces, remains in dust, and becomes embedded in environments where secondhand smoke (SHS) has been released into the air. Even when parents are diligent in attempting to shield their children from tobacco smoke, exposure to SHS (SHSe) and THS (THSe) still occurs. Residue from previously smoked tobacco at home or in a car creates a pervasive reservoir of tobacco smoke pollutants that are within reach of a child's hand such as on carpets, furniture, clothes, and toys, and breathed in dust. Homes of smokers become reservoirs of these pollutants that persist for years, become more toxic with age, and are later reemitted into the gas phase, or react with common ambient oxidants and other environmental compounds to yield secondary pollutants such as carcinogenic tobacco-specific nitrosamines. The clinical effects of THSe are unknown because prior research has examined children exposed to both SHS and THS. Studies exclusively focusing on THSe are needed. Thus, we have conducted in-vitro, animal, and pilot pediatric studies that demonstrate that THSe is associated with high levels of inflammatory cytokines, respiratory illnesses, and oxidative stress including DNA damage, in mice. We have found even in the presence of smoking bans, children still have high levels of THS pollution on their hands and that nonsmokers' homes have high THS pollution levels. However, in the absence of large-scale, rigorous human studies, conclusions about the clinical effects of THSe cannot be made. Thus, we propose an innovative prospective longitudinal cohort study that will move the field forward and away from the laboratory to a pediatric clinical setting as the first pediatric study to use biochemical validation to identify children exposed to THS-only over time. We will screen 1000 children from the pediatric emergency department, a setting which cares for children with varying tobacco smoke exposure (TSE) levels and illnesses. Using strict screening and chemical analysis techniques, we will identify and compare children that comprise three distinct TSE groups: 1) THSe only group: live with nonsmokers, no reported SHSe, confirmed negative/low levels of SHSe, elevated levels of THSe; 2) Mixed SHSe+THSe group: live with smokers, reported SHSe, confirmed moderate/high levels of SHSe, high levels of THSe; and 3) No TSE group: live with nonsmokers, no reported SHSe, confirmed negative levels of SHSe and THSe. The prevalence and levels of THSe, demographics, and exposure and illness patterns of these groups will be compared over time. Next, we will disentangle which environmental sources contribute to THSe levels and the association between THSe and inflammatory (i.e., cytokines) and oxidative (i.e., DNA, lipid, protein oxidation) biomarkers and TSE- related clinical illnesses. Results will provide unique insights into how THSe and sources of tobacco smoke pollution affect the inflammatory, oxidative, and clinical responses in children. The potential impact of these findings is substantial as currently, the level of clinical risk attributable to THSe is unknown.